The Effect of Anti-TNF Therapy on Cardiac Function in Rheumatoid Arthritis: An Observational Study.

Milad Baniaamam,Rabia Agca,M Louis Handoko,Thelma C Konings,Mike T Nurmohamed,Vokko P Van Halm,Sjoerd C Heslinga

doi:10.3390/jcm9103145

Abstract

Congestive heart failure (CHF) is the second most prevalent cause of death in rheumatoid arthritis (RA). The systemic inflammatory state in RA patients is deemed responsible for this finding. Anti-inflammatory treatment with anti-tumor necrosis factor (anti-TNF) therapy decreases CV risk and subsequently might improve the cardiac function by lowering the overall inflammatory state. This study investigated the effect of anti-TNF on the cardiac function in RA patients. Fifty one RA patients were included, of which thirty three completed follow-up. Included patients were >18 years, had moderate–high disease activity and no history of cardiac disease. Patients were assessed at baseline and after six months of anti-TNF treatment. Patients underwent conventional Speckle tracking and tissue Doppler echocardiography in combination with clinical and laboratory assessments at baseline and follow-up. The left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) showed no changes during follow-up, LVEF 63% (±9) to 62% (±8) p = 0.097 and GLS −20 (±4) to −20 (±3) p = 0.79, respectively. Furthermore, E/e’ nor E/A changed significantly between baseline and follow-up, respectively 8 (7–9) and 8 (7–9) p = 0.17 and 1.1 (±0.4) and 1.1 (±0.4) p = 0.94. Follow-up NT-proBNP decreased with 23%, from 89 ng/L (47–142) to 69 ng/L (42–155), p = 0.10. Regression analysis revealed no association between change in inflammatory variables and cardiac function. Echocardiography showed no effect of anti-TNF treatment on the cardiac function in RA patients with low prevalence of cardiac dysfunction. Moreover, NT-proBNP decreased, possibly indicating (subtle) improvement of the cardiac function.

Highlights

Patients with rheumatoid arthritis (RA) have a 1.5-fold increased risk of cardiovascular (CV) mortality [1,2]
The latter is possibly explained by a process in which circulating pro-inflammatory mediators, such as tumor necrosis factor (TNF), induce coronary endothelial activation leading to stiffness of the myocardium and interstitial fibrosis deposition, resulting in impairment of the relaxation of the myocardium [7]
This study aimed to elucidate the effect of anti-inflammatory therapy, i.e., anti-TNF, on the systolic and diastolic cardiac function in RA patients assessed with comprehensive echocardiography and cardiac biomarkers

Summary

Introduction

Patients with rheumatoid arthritis (RA) have a 1.5-fold increased risk of cardiovascular (CV) mortality [1,2]. A direct effect of the systemic inflammation itself has been suggested as a cause for the development of left ventricular (LV) dysfunction The latter is possibly explained by a process in which circulating pro-inflammatory mediators, such as tumor necrosis factor (TNF), induce coronary endothelial activation leading to stiffness of the myocardium and interstitial fibrosis deposition, resulting in impairment of the relaxation of the myocardium (diastolic dysfunction) [7]. RA studies have shown an increased prevalence of left ventricular diastolic dysfunction [8,9,10] This explanation is underlined by studies demonstrating that the increased incidence of CHF is only partly due to increased prevalence of CV risk factors, such as hypertension, dyslipidemia and increased insulin resistance. Even after correction for these traditional risk factors, the increased risk for CHF remains [11,12]

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